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2 - CR/MET > CR PBLs > Flashcards

CR PBLs Flashcards

1
Q

Types of CoA

A

Pre-ductal
Juxtaductal
Post-ductal

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2
Q

Which type of CoA is most common?

A

Juxtaductal

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3
Q

Defects associated with CoA

A

Left sided obstructive defects
VSD
Bicuspid aortic valve
Aortic arch hyperplasia

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4
Q

Surgical treatments for CoA

A

Resection and end-end anastomosis
Patch aortoplasty
Left subclavian flap angioplasty
Bypass graft repair

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5
Q

Symptoms of second degree heart block

A

Lightheadedness, dizziness, syncope
Chest pain
Irregular heart beat
Bradycardia

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6
Q

Causes of heart block

A 
Electrolyte imbalances 
MI 
Coronary artery disease
Myocarditis or cardiomyopathy 
Heart enlargement from heart failure
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7
Q

Indications for pacemaker in heart block

A

Persistant bradycarida
Asystole for >3 seconds
Heart failure
Associated with neuromuscular disease

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8
Q

When is CRP commonly raised?

A

Late pregnancy
Mild inflammation
Bacterial and viral infection
Burns

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9
Q

Reversible risk factors or angina

A 
Smoking 
Hypertension 
Hyperlipidameia 
Obesity 
Physical inactivity
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10
Q

Irreversible risk factors for angina

A

Family history
Older age
Male sex
Diabetes mellitus

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11
Q

Signs of angina on ECG stress test

A

ST depression
T wave inversion
Short and spikey T waves

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12
Q

Drugs used in angina treatment

A 
Aspirin
CCBs
BBs
Statins 
Nitrates 
Beta blockers 
ACEIs
ARBs
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13
Q

Characteristics of unstable angina

A

Pain comes on suddenly
Not triggered by exertion
Does not go away with rest
Gets worse over a short period of time

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14
Q

ST elevation

A

= ongoing active damage
>2mm in chest leads
>1mm in limb leads
Must be present in 2 or more contiguous leads

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15
Q

Pathological Q waves

A 
= irreversible damage 
>0.04s
>2 small squares in depth 
>25% of the depth of the QRS complex 
Present in V1-3
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16
Q

Troponin subtypes

A

T and I

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17
Q

When is troponin released and when do levels return to normal?

A

First released 4-6 hours after attack

May remain elevated for 2 weeks

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18
Q

Myocardial creatine kinase

A

= CK-MB

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19
Q

When is CK released and when do levels return to normal?

A

3-12 hours after infarct

Return to normal after 48-72 hours

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20
Q

When is AST released and when do levels return to normal?

A

Peaks around 48 hours

Returns to normal after 5 days

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21
Q

When is LDH released and when do levels return to normal?

A

Peaks around 72 hours

Returns to normal after 6 days

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22
Q

When is myoglobin released?

A

As early as 2 hours after infarct

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23
Q

Pain felt in AMI

A 
Intense and consistent for 30-60 minutes
Retrosternal
Radiates --> neck, jaw, back, arm
May be felt as indigestion 
Felt as a weight on the chest as squeezing pain
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24
Q

AMI immediate treatment

A

Aspirin
Pain relief and sedation
Thrombolysis or PCI
Beta blockers

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25
Q

Secondary prevention

A

Aspirin
Beta blocker
Statin
ACEI

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26
Q

Short term complications of AMI

A

Arrhythmia
Heart failure
Rupture
Mural thrombosis

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27
Q

Long term complications of AMI

A

Aneurysm
Heart failure
Pericarditis

28
Q

Adverse prognostic features of AMI

A 
Advanced age 
Anterior AMI 
Larger AMI 
Heart failure 
Systolic hypotension 
Complex ventricular arrhythmias >24h after infarct 
History of previous infarct(s)
29
Q

Causes of heart failure

A 
Coronary artery disease
Valve disease
Cardiomyopathy 
Congenital defects
Toxins (alcohol, cocaine)
Drugs (BBs, CCBs) 
Anaemia 
Pregnancy 
Hyperthyroidism
30
Q

Major criteria for heart failure

A 
PND
Weight loss with treatment 
Neck vein distention 
Hepatojugular reflux 
Rales 
S3 gallop 
Cardiomegaly
31
Q

Minor criteria for heart failure

A 
Nocturnal cough 
Dyspnoea on normal exertion 
Decrease in VC by 1/3 
Pleural effusion 
Tachycardia 
Bilateral ankle oedema
32
Q

Why do you get PND?

A

Return of peripheral oedema fluid to circulation due to gravity
Reduced respiratory drive during sleep
Reduced sympathetic bronchodilation during sleep

33
Q

ECG features of heart failure

A

LVH (high R waves in V4-6)
ST depression showing ischaemia
LBBB

34
Q

CXR findings

A 
Cardiomegaly 
Bat wing sign
Kerley B lines 
Pleural effusions 
Upper lobe diversion
35
Q

Echo findings

A 
Reduced eject fraction 
Dilated ventricles 
Valve dysfunction 
Pulmonary artery pressure raised 
Reduced/increased wall thickness
36
Q

Drugs for heart failure

A 
Diuretics 
ACEIs
Beta blockers 
ARB
Aldosterone blocker 
Digoxin
37
Q

Heart failure prognosis

A

50% die within 5 years

38
Q

Asthma characteristics

A

Airflow limitation
Airway hyper responsiveness
Inflammation on bronchi

39
Q

Raised cells in asthma

A

Eosinophils
Mast cells
T cells

40
Q

Signs of severe asthma

A 
SaO2 <92% 
PEFR <33% predicted 
Tachycardia 
PaO2 <8kPa 
PaCO2 normal or raised
Silent chest 
Cyanosis 
Inability to complete sentences in one breath 
Feeble respiratory effort
41
Q

Treatment ladder of asthma

A 
Salbutamol 
Inhaled steroid 
LABA 
Leukotriene antagonist
Antimuscarinic  
Theophylline 
Oral steroid
42
Q

Risk factors for DVT

A 
Previous DVT 
Hospitalisation 
Surgery 
Active cancer 
Lower limb trauma 
Increasing age 
Pregnancy 
COCP/HRT 
Obesity 
Thrombophilia 
Long haul travel 
Family history
43
Q

Signs and symptoms of DVT

A 
Limb pain 
Tenderness
Swelling 
Pitting oedema 
Distention of superficial veins 
Increased temperature 
Erythema 
Cord like palpable vein
44
Q

What is D dimer?

A

Breakdown product of cross-liked fibrin produced by plasmin

45
Q

DVT treatment

A

LMWH then warfarin

46
Q

Complications of DVT

A

PE
Active bleeding from treatment
Post-thrombotic syndrome
Heparin induced thrombocytopaenia

47
Q

Forms of embolus

A 
DVT 
Fat 
Air 
Amniotic fluid 
Tumour
48
Q

Symptoms of PE

A

Dyspnoea
Pleuritic chest pain
Haemoptysis

49
Q

Atypical symptoms of PE

A 
Syncope 
Seizures 
Abdominal pain 
Fever
Confusion 
Delirium
50
Q

Signs of PE

A 
Tachycardia 
Tachypnea 
Hypoxia 
Pyrexia 
Raised JVP 
Pleural rub 
Accentuated second heart sound 
Hypotension and shock
51
Q

Differential diagnosis of PE

A 
Pneumonia 
Acute coronary syndrome 
Aortic dissection 
Cardiac tamponade 
Pneumothorax
52
Q

ECG signs of PE

A 
Tachycardia 
RBBB
RV strain 
RAD 
Large P waves 
S1Q3T3 pattern 
Atrial arrhythmia
53
Q

CXR signs of PE

A 
Dark lung fields 
Focal oligaemia 
Prominent central artery 
Basal wedge shaped opacities 
Pleural effusion
54
Q

Type of respiratory failure in PE

A

1

55
Q

Treatment of PE

A

Heparin or fondaparinux
Then warfarin
Thrombolysis in massive PE

56
Q

Can thrombolysis be used in pregnancy?

A

YES

57
Q

Sites of RBC production

A

Yolk sac
Liver and spleen
Bone marrow

58
Q

Forms of haemoglobin

A

Hb Gower 1 = zeta 2 epsilon 2
HbF = alpha 2 gamma 2
HbA = alpha 2 beta 2
HbA2 = alpha 2 delta 2

59
Q

Genetics of alpha thalassaemia

A

Gene deletions on chromosome 16

Usually 4 genes present

60
Q

Consequences of alpha thalassaemia

A

1-2 deletions = no symptoms
3 deletions = HbH disease –> severe microcytic anaemia
4 deletions = hydrops foetalis –> death

61
Q

Hb levels in beta thalassaemia major

A

Low HbA
High HbF
Normal or slightly high HbA2

62
Q

Sites of extra medullary haematopoiesis

A

Spleen

Liver

63
Q

Consequences of haemolysis

A

Jaundice
Reticulocytosis
Hepatosplenomegaly

64
Q

Treatment of beta thalassaemia major

A

Regular blood transfusions
Iron chelation therapy
Bone marrow transplant
Splenectomy

65
Q

Iron chelating agents

A

Desferrioxamine (SQ)

Deferiprone (oral)

2 - CR/MET (8 decks)

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